Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells that expand during cancer, inflammation, and infection, and have a significant ability to suppress T-cell responses. These cells play a crucial role in regulating immune responses in both healthy individuals and various diseases. This review discusses the origin, mechanisms of expansion, and suppressive functions of MDSCs, as well as potential therapeutic strategies to target these cells. MDSCs are characterized by their myeloid origin, immature state, and ability to suppress T-cell responses. They lack specific surface markers and consist of a mixture of granulocytic and monocytic morphology. MDSCs are expanded in pathological conditions, such as cancer, bacterial and parasitic infections, acute and chronic inflammation, and autoimmune diseases. The expansion of MDSCs is influenced by factors produced by tumor cells and activated T cells, which promote myelopoiesis and inhibit the differentiation of mature myeloid cells. STAT3 is a key transcription factor regulating MDSC expansion. MDSCs produce reactive oxygen species (ROS), nitric oxide (NO), and arginase, which contribute to their suppressive activity. Recent studies have also identified peroxynitrite as a crucial mediator of MDSC-mediated T-cell suppression. Different subsets of MDSCs, such as granulocytic and monocytic subsets, use distinct mechanisms to suppress T-cell proliferation. MDSCs can also induce the de novo development of regulatory T (Treg) cells. Therapeutic targeting of MDSCs includes promoting myeloid-cell differentiation, inhibiting MDSC expansion, and blocking their function. Vitamin A metabolites, such as retinoic acid, have been shown to promote the differentiation of MDSCs into mature myeloid cells. Inhibiting factors that promote MDSC expansion, such as stem-cell factor (SCF) and vascular endothelial growth factor (VEGF), can reduce MDSC numbers. Inhibiting the production of suppressive factors, such as arginase and iNOS, can also enhance antitumor immune responses. Direct elimination of MDSCs using chemotherapeutic drugs has shown promising results in reducing their numbers and improving anti-tumor responses. The role of MDSCs in chronic infections and cancer is distinct from their role in acute conditions, where they contribute to immunosuppression at tumor sites. MDSCs may function as regulatory components of the immune system, preventing pathological immune-mediated damage. Further research is needed to understand the specific subsets of MDSCs involved in T-cell suppression and the molecular mechanisms responsible for their suppressive functions.Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells that expand during cancer, inflammation, and infection, and have a significant ability to suppress T-cell responses. These cells play a crucial role in regulating immune responses in both healthy individuals and various diseases. This review discusses the origin, mechanisms of expansion, and suppressive functions of MDSCs, as well as potential therapeutic strategies to target these cells. MDSCs are characterized by their myeloid origin, immature state, and ability to suppress T-cell responses. They lack specific surface markers and consist of a mixture of granulocytic and monocytic morphology. MDSCs are expanded in pathological conditions, such as cancer, bacterial and parasitic infections, acute and chronic inflammation, and autoimmune diseases. The expansion of MDSCs is influenced by factors produced by tumor cells and activated T cells, which promote myelopoiesis and inhibit the differentiation of mature myeloid cells. STAT3 is a key transcription factor regulating MDSC expansion. MDSCs produce reactive oxygen species (ROS), nitric oxide (NO), and arginase, which contribute to their suppressive activity. Recent studies have also identified peroxynitrite as a crucial mediator of MDSC-mediated T-cell suppression. Different subsets of MDSCs, such as granulocytic and monocytic subsets, use distinct mechanisms to suppress T-cell proliferation. MDSCs can also induce the de novo development of regulatory T (Treg) cells. Therapeutic targeting of MDSCs includes promoting myeloid-cell differentiation, inhibiting MDSC expansion, and blocking their function. Vitamin A metabolites, such as retinoic acid, have been shown to promote the differentiation of MDSCs into mature myeloid cells. Inhibiting factors that promote MDSC expansion, such as stem-cell factor (SCF) and vascular endothelial growth factor (VEGF), can reduce MDSC numbers. Inhibiting the production of suppressive factors, such as arginase and iNOS, can also enhance antitumor immune responses. Direct elimination of MDSCs using chemotherapeutic drugs has shown promising results in reducing their numbers and improving anti-tumor responses. The role of MDSCs in chronic infections and cancer is distinct from their role in acute conditions, where they contribute to immunosuppression at tumor sites. MDSCs may function as regulatory components of the immune system, preventing pathological immune-mediated damage. Further research is needed to understand the specific subsets of MDSCs involved in T-cell suppression and the molecular mechanisms responsible for their suppressive functions.